The kidneys appear to play a role in shifting N from ureogenesis to gln synthesis in metabolic acidosis. The mechanism(s) responsible for this shift as well as for maintenance of gln and glucose homeostasis during acidosis are the long-term goals of this study. Evidence supporting a N distribution shift comes from the partitioning of urinary N as well as hepatoportal concentration differences measured in situ. Thus in metabolic acidosis, induced by either NH(4)Cl of HCl, the per cent of urinary N (NH(4)+urea) excreted as NH(3) rises from 2-5 in controls to 25-36 in acidosis. Direct evidence for hepatic involvement in N partition comes from the fall in urea and rise inglutamine release in acidosis. A new methological approach, regional blood flows measured by the pulsed Doppler Effect will provide for the first time in rat quantitative estimates of organ extraction/production rates; this approach not only constitutes a tremendous cost savings over large animal studies but also may be adapted for chronic studies. From the perspective or interorgan control this N shift could be affected by either kidney/muscle or gut/liver interactions. Renal venous HH(3) release (increased in acidosis) could favor muscle gln production at the expense of ala thereby depriving liver of a ureogenic precursor (ala) while sustaining renal NH(3) synthesis (gln). Portal drained viscera NH(3) release, at the expense of ala, appears to supply in a feed-forward fashion N in a form preferentially converted to gln. The relative quantitative contributions of both can be assessed using blood flow (hind limb and hepatic) and (A-V) of the major N carriers, NH(3) gln, glu, ala and urea. Renal influence on N distribution is seen in bilateral ureteral ligated acidotic rats which shifts urinary NH(3) to the renal venous release. In this condition NH(3)-N is incorporated into gln (muscle) and subsequently transformed into ala (gut) and finally deposited into urea (liver). The role of NH3 as a precursor or as a possible metabolic regulator (proteolysis) will be sutdied using the stable isotope 15N and measuring the differential incorporation into gln and urea (arterial as well as muscle and hepatic sites); a comparison of glutamine carbon, 14C, and nitrogen, 15N, turnover rates should provide insight into recycling. Kidneys may influence both glutamine and glucose homeostasis via renal NH3 release.